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Systems of Neuroscience > Unit 1 > Flashcards

Unit 1 Flashcards

1
Q

Neuroscience

A

study of how neural cells operate within complex networks resulting in integrative functions such as vision

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2
Q

Why is neuroscience important?

A
  • body homeostasis
  • neurological conditions
  • promote wellbeing
  • developing technnology
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3
Q

Neuronal structure

A

CNS & PNS

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4
Q

CNS consists of

A

brain
spinal cord

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5
Q

PNS consists of

A

extremities

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6
Q

Neural cell types

A

neuronal cells
glial cells

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7
Q

Neuronal cells

A

AKA neurons, functional unit of nervous system

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8
Q

Glial cells

A

supporting role (don’t fire APs)

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9
Q

Commonalities between neuronal cell types

A

cell body (soma)
long processes

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10
Q

Dendrites

A

receive info
highly branched

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11
Q

Axon

A

Transmits info
(note: diff lengths in diff neurons, could have branches (axon collaterals), axon terminal forms synapse)

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12
Q

Myelin sheath

A

-fatty
-produced by glial cells
-glial cells in CNS = oligodendrocytes
-glial cells in PNS = neurolemmocytes/ schwann cells

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13
Q

Schwann cells/ neurolemmocytes

A

in PNS
need multiple to insulate 1 PNS neuron

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14
Q

Oligodendrocytes

A

in CNS
1 can insulate up to 110 neurons at a time

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15
Q

PNS contains

A

afferent and efferent neurons

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16
Q

Afferent neuron senses

A

-how stimulus affects you
-somatic sensory (touch/pain)
-visceral sensory (organs)
-Special sensory (hear/sight/taste)

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17
Q

Efferent neuron motor functions

A

-how stimulus effects you
-somatic motor (voluntary)
-autonomic motor (HR)

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18
Q

Afferent neurons

A
  • have only axon no dendrites
  • info doesn’t go through cell body
  • detect change
  • generate signal
  • propagate to CNS
  • cell body sits in PNS and extends into CNS
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19
Q

Interneurons

A
  • varied morphology
  • 99% of all neurons
  • integrate info
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20
Q

efferent neurons

A
  • transmits signal away from CNA
  • initiate action (sweat, movements, etc)
  • cell body sits in CNA and extends into PNS
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21
Q

Neuronal communication

A
  • electrical signal is changed into CS to jump gaps @ synapse
  • pre-synaptic neuron = axon terminal/ synaptic terminal (has vesicles)
  • post-synaptic neuron = dendrite usually
  • Steps: 1. transmission 2. reception 3. integration
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22
Q

Glial Cell function

A

metabolic and physical support provided by glial cells

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23
Q

Microglia

A

glial cell, immune support
astrocytes in subventricular zone can rise to more: stem cells, mature astrocytes or oglios, neurons

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24
Q

Glial stem cells

A

capable of differentiating into glial cells and neurons too (brain can make new neurons)

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25
Q

CNS cell bodies

A

nucleus: accumulation of neuron cell bodies in CNS

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26
Q

CNS axons

A

Tracts: bundles of neuronal axons many of which are enveloped by glial cells of CNS

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27
Q

PNS cell bodies

A

ganglia: local accumulation of nerve cell bodies and supporting cells

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28
Q

PNS axons

A

Nerves: bundles of peripheral axons many of which are enveloped by glial cells of PNS

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29
Q

Gray matter of CNS

A
  • no myelin
  • nucleus: accumulation of neurons w/ similar connections & functions
  • cortex: sheet-like arrays of nerve cells
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30
Q

Neural systems serve 3 purposes:

A
  1. sensory systems report the state of the organism and its environment
  2. Motor systems organize and generate actions
  3. Associated systems integrate information
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31
Q

Cognition broadly defined as…

A

Perception, attention, memory, emotions, language, and thinking

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32
Q

Synapses

A

Junction between neurons where information is passed from one to the other; typically, a chemical synapse where a physical cleft exists between communicating neurons, but could also refer to electrical synapses mediated by gap junctions

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33
Q

Discovery of neurons and glial cells found that

A

neurons are specialized for sending electrical signals due to specific features and molecules in diff. parts of cell. The variety of glial cells and neurons explains why the nervous system is so complex

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34
Q

Electrical synapses

A

synapses that transmit information via the direct flow of electrical current at gap junctions

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35
Q

Functions of gap junctions

A

allow for cytoplasmic continuity and transfer of electrical and chemical signals between cells in the nervous system

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36
Q

Synaptic Vesicles

A

In presynaptic neuron, fuse with PM to release NTs (exocytosis)

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37
Q

How do neurotransmitters act on postsynaptic neurons?

A

NTs activate postsynaptic specializations (characterized by concentration of NT receptors that detect NTs) either on adjacent dendritic regions in the CNS or target tissues (muscles and glands) in the PNS

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38
Q

More dendritic arbors =

A

More possible responses in a target neuron and more reliablity

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39
Q

Convergence

A

Innervation of a target cell by axons from more than one neuron. Ex: vision, convergence of both rod and cone photoreceptor cells onto retinal ganglion cells

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40
Q

Divergence

A

Axons can make connections to multiple target neurons, if an axon only innervates one target cell it is minimally divergent

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41
Q

Glial cells

A

surround axons and dendrites, have processes but are different from neurons, are highly responsive to brain injury, and are only stem cells retained in the mature brain

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42
Q

Functions of Glial Cells

A

maintain ionic milieu of nerve cells, modulate rate of nerve signal propagation (myelination), modulate synaptic action by controlling uptake and metabolism of NTs at or near synaptic cleft

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43
Q

Astrocytes

A

Only in CNS, type of glial cell. Maintain an appropriate chemical environment for neuronal signaling (BBB); recently found that they can secrete substances that influence new synaptic connections

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44
Q

Electrical Signaling in the brain

A
  • estimated one neuron can receive input from 10,000 other cells
  • one neuron could contact up to 10,000 others
  • complexity of the neural network is vast
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45
Q

How are APs modulated?

A

Pulse frequency:
- longer duration/ higher magnitude stimuli result = initiation of multiple APs
- more intense stimulus = more frequency of APs generated
- info in AP is encoded in frequency not amplitude
- Maximum frequency of APs is dictated by absolute refractory period

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46
Q

Synaptic Potential

A
  • Potential is diff. across post-synaptic membrane
  • Can be excitatory (EPSP) or inhibitory (IPSP)
  • Dependent on release of NT from pre-synaptic neuron
  • Generally smaller in amplitude (many needed to trigger an AP)
  • Slower time course
  • Do not have refractory period
  • Degrade quickly as they move away from synapse

Afferent neuron will never generate synaptic potential bc it will always be pre-synaptic neuron

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46
Q

Receptor Potential

A

Receptor activated by pressure on the skin (Pacinian Corpuscle)

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47
Q

Action Potential

A

All neurons fire APs

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48
Q

Three types of electrical signaling in the brain

A
  1. Receptor Potential
  2. Synaptic Potential
  3. Action Potential
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49
Q

Setting up Synaptic Potentials

A
  1. APs in excitatory presynaptic neuron causes depolarization of the blue post-synaptic neuron
  2. Depolarization is an excitatory post synaptic potential
  3. A single AP in a presynaptic cell is not enough to produce an EPSP large enough to reach threshold and trigger an A

EPSPs increase likelihood of AP firing in postsynaptic neuron (IPSPs decrease likelihood of AP firing)

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50
Q

Temporal Summation

A

Multiple synaptic potentials add up to reach the threshold and trigger an AP

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51
Q

IPSP (Inhibitory Postsynaptic Potenial)

A

Consequence of AP in inhibitory presynatic neuron is to decrease (hyperpolarize) the membrane potential of the post-synaptic neuron

now the membrane potential is more negative than it was before- so it is farther away from the threshold

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52
Q

Synaptic Integration

A
  • IPSP and EPSPs added up (temporal summation = timing of APs, spatial summation = are of dendrites receiving them)
  • If sum of inputs is above threshold, AP fires
  • If sum is below threshold, no AP initiated
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53
Q

Synaptic Integration Example

A
  1. If 2 excitatory signals are received the summating EPSPs cause an AP to fire
  2. If an IPSP from an inhibitory neuron occurs just before the APS from the excitatory neuron, the summation of the one negative IPSP and 2 EPSPs is not enought to reach threshold and AP is not generated

inhibitory neurons are important for regulating ability of excitatory signal to trigger AP in post synaptic cell; huntington’s disease is an example of how this can be a problem

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54
Q

Feedforward Excitation

A
  • Can be drawn with 2 neurons
  • allows one neuron to relay info to its neighbor
  • long chains of these used to propagate info through nervous system
55
Q

Feedforward Inhibition

A
  • need to draw 3 neurons
  • presynaptic cell excites an inhibitory interneuron and that inhibits the following post synaptic cell
  • Way of shutting down or limiting excitation in downstream neuron in neural circuit
56
Q

Convergence/Divergence

A

One postsynaptic cell receives converging signals from several different presynatic cells and any individual neuron can make diverging connections to many diff. postsynaptic cells

57
Q

Lateral Inhibition

A

Presynaptic cell excites inhibitory interneurons and they inhibit neighboring cells in the network; this type of circuit is used in sensory systems

58
Q

Feedback/Recurrent Inhibition

A
  1. Feedback Inhibition: presynaptic cell connects to a postsynaptic cell and that cell in turn connects to an interneuron which then inhibits the presynaptic cell
  2. Recurrent Inhibition: each neuron in the closed chain inhibits the neuron to which it is connected
59
Q

Feedback/Recurrent Excitation

A
  • Feedback Excitation: a presynaptic neuron excites a postsynaptic neuron and that neuron excites the presynaptic neuron
  • Recurrent Excitation: variant of feedback excitation in which a presynaptic neuron excites a postsynaptic neuron that can feedback to excite itself (an autapse) or other neurons which ultimately feedback to itself
60
Q

Reflexes

A
  1. tap of hammer stretches muscle
  2. initiates APs in sensory neurons (afferent)
  3. APs propagate to spinal cord where the axon splits (bifurcates) into two branches
  4. One branch makes a direct synaptic connection with a motor neuron (this excites the motor neuron and an AP is generated in the motor neuron, leading to contraction of the extensor muscle and the leg to kick out)- feedfoward excitation loop
  5. other branch of the sensory neuron axon synapses with an interneuron, causing an AP to fire in the interneuron
  6. the interneuron generates an IPSP in the motor neuron for the flexor muscle (this decreaes the probability of the flexor motor neuron becoming active and producing an inappropriate flexion of the leg)- feedforward inhibition
61
Q

Convergence and Divergence in Reflexes

A

Divergence: single sensory neuron has multiple branches that diverge and synapse with many individual motor neurons
Convergence: multiple sensory neurons are activated and these neurons all projet into the spinal cord where they converge on to individual extensor motor neurons

62
Q

Lateral Inhibition

A

important for processing sensory info

63
Q

Lateral Inhibition is used in Edge Enhancement

A

Looking at light and dark grey side by side the border on the dark side looks darker and lighter on light side. The border is the same shade though.
- light falls on retina
- intensity of light described by step-like gradient (dark gray = 10 units of intensity, light gray= 5 units of intensity)
- gradient of light activates photoreceptors which connect to neurons
- 10 units of intensity =10 AP spikes, same with 5 units = 5 AP spikes
- without lateral inhibition then gradient perceived is exactly same as gradient of light intensity

64
Q

How lateral inhibition works during edge enhancement

A
  • 0.2x inhibitory strength on each neighbor (10 units stimulation = 2 units inhibition)
  • neurons with stimuli away from border receive same excitation and inhibition
  • at border however, levels of inhibition change due to difference in light intensity on each side of border
  • information transmitted to nervous system and gradient perceived enhances border
65
Q

Feedback inhibition example:

A
  • axon of an alpha motor neuron branches
  • one branch innervates muscle
  • another branch makes an excitatory synapse with an interneuron called the renshaw cell
  • renshaw cell (interneuron) inhibits motor neuron to close loop
  • Important to prevent excessive output from motor neurons
66
Q

Recurrent excitation in hippocampus

A
  • 6 hippocampal pyramidal neurons (U-Z) receive presynaptic connection from neurons (a-f), the presynaptic neurons could be active or inactive
  • neuron a activates neuron Z and produces one output
  • neurons U-Z have axon collaterals that connect with themselves and the other 4 pyramidal neurons called a matrix of connectivity (recurrent excitation)
  • every neuron receives convergent info from all other neurons and also diverging outputs to all other neurons
67
Q

Hebb Learning Rule

A

Synapse will change its strength if that synapse is active and post-synaptic cell is active at same time

this learning rule plus recurrent excitation causes interesting results

68
Q

Recurrent excitation in memory

A

memory is not one synapse changing, it is distributed in network

69
Q

Specific neural microcircuits

A
  • feedforward excitation/inhibition
  • convergence/ divergence
  • lateral inhibition
  • recurrent excitation/inhibition
70
Q

Body sense (touch)

A

representation of body in brain
2 major component inputs
- mechanical
- pain and temp
use these to:
- identify shape and texture
- monitor forces
- detect potentially harmful stimuli

71
Q

Afferent fibres

A
  • from PNS to CNS
  • cell bodies in ganglia (collection of cell bodies)
  • critical links between body and outside world
  • dorsal root ganglia (for body on the back)
  • Cranial nerve ganglia (for head)
  • Singular process that is continuous between central and peripheral process (pseudounipolar)
72
Q

Signal Transduction (touch)

A
  • convert mechanical force into electrical signal
  • called sensory transduction
  • receptor potential: depolarizing current resulting from a stimulus opening an ion channel in afferent nerve endings
  • Merkel cells express Piezo2 ion channels which open as a result of mechanical stimuli
  • if sufficient in magnitude, receptor potential will reach threshold for generation of APs
73
Q

Different types of touch

A
  • texture
  • pressure
  • hard/soft
74
Q

Sensory Receptors

A
  • Meisner (tactile) Corpus
  • Pacinian Corpuscle
  • Merkel Cells
  • Ruffini Corpuscle
  • Free nerve endings

muscle spindle - proprioception

75
Q

Ruffini Corpuscle

A
  • heavy touch
  • located in dermis
76
Q

Pacinian Corpuscle

A
  • detects pressure stretch
  • rapidly adapting
  • in dermis
76
Q

Meisner (tactile) corpus

A
  • detects light touch
  • in palm of hands
  • rapidly adaptive
77
Q

Merkel Cells

A
  • detect texture and edges
  • in epidermis
78
Q

Free Nerve Endings

A
  • widespread location
  • detect pain + temp
79
Q

Afferent Fiber Classes: Axonal Subtypes

A
  • classified by conduction velocity
  • large diameter= faster conduction
  • Axons from skin designated by letters (A is fastest and largest, C is slowest and smallest; A group further divided by greek letters- alpha fastest then beta then delta)
  • axons from muscles designated by roman numerals (I is largest and fastest, II, III, IV slowest; subgroups with lowercase roman letters)
80
Q

Afferent fiber classes: temporal dynamics

A
  • slowly adapting (continue to respond as long as stimulus is present, gives info about persistance of stimulus or its spatial attribute- shape and size)
  • Rapidly adapting (informs about changes in stimulus-movement; fire rapidly at first then become quiescent w/ continued stimulus) - like wearing a shirt
81
Q

White and Gray Matter of CNS

A
  • gray matter (primarily cell bodies and dendrites)
  • White matter (primarily myelinated axons)
  • in spinal cord white matter is more external, brain is opposite
82
Q

Ganglia

A
  • nerve is several axons wrapped by connective tissue
  • nerves found in PNS (no nerves in CNS)
  • Ganglion (ganglia plural) is cluster of neuron cell bodies along nerve
  • reuslts in bulging of nerve where ganglia is located
83
Q

Gray Matter of Spinal Cord

A

Dorsal:
- posterior horn - sensory info, axons of sensory neruons, cell bodies of interneurons
- lateral horn - visceral motor info, cell bodies of autonomic motor neurons, only found in T1-L2 parts of spinal cord
- Anterior horn - somatic motor info, cell bodies of somatic motor neurons
Ventral:
- Gray commissure: communication between R+L, unmyelinated axons

axons w/in white matter of area of each horn organized into tracts

84
Q

Spinal Tracts

A
  • ascending tracts: carry sensory info to brain
  • descending tracts: carry motor info from brain
  • ipsilateral tracts: dont cross midline
  • contralateral tracts: cross midline
85
Q

Somatosensory Projections from body

A

2 routes for sensory info:
1. medial lemniscal pathway: mechanoreceptive and proprioceptive
2. spinothalamic tract: pain and temp
Typically travels through 3 neuorns:
- first order neurons ascend through dorsal colum to dorsal column nuclei (can be afferent)
- second order neurons relay signal to thalamus (cross midline so are commissural)
- third order carry signal from thalamus to cortex

axons enter dorsal root; bifurcate into ascending and descending branches (still part of ascending tracts)

86
Q

Somatosensory Projections: direct pathway

A
  • main ascending branch extends ipsilatereally through dorsal column
  • synapse on neurons in dorsal column nuclei in medulla
87
Q

Somatosensory Projections: Indirect Pathway

A
  • projection neurons in dorsal horn receive inputs from collaterasl
  • project in dorsal colum to same dorsal column nuclei
  • sometimes called postsynaptic dorsal column projection
88
Q

Somatosensory Projections: Organization

A

Dorsal columns are topographically organized
- lower limb info: more medial before decussation, Graclie Tract
- Upper limb info: more lateral before decussation, Cuneaute Tract
2nd order neurons:
- Go from dorsal column nuclei to thalamus (called Internal Arcuate Fibers)
- Cross midline to form medial lemniscus
- upper body fibers become medial and lower body fibers become lateral
- Synapse with thalamic neurons in ventral posterior lateral nucleaus (VPL)
- VPL receives input from contralateral dorsal column (hurt right leg, info received on L side of VPL)
3rd Order Neurons
- VPL to inernal capsule to postcentral gyrus
- poscentral gyrus is known as primary somatosensory cortex (SI)

Somatosensory cortex represents mechosensory signals first generated in cutaneous surfaces of contralateral body

89
Q

Dermatome

A
  • sensory ganglion innervate a specific region of skin (each dorsal root ganglion spinal cord associated with parts of skin)
  • region arisesduring embryonic development
  • Each DRG associated with specific region of skin
  • Organization same in all humans
  • important for diagnosis of suspected spinal injuries

areas occupied by different regions in cortex are not proportional to size

90
Q

Fine topographic map

A

Areas occupied by different regions in the cortex are not proportional to their size

91
Q

Receptive Fields

A
  • each sensory neuron has a receptive field
  • size of receptive field can be measured by assessing ability to discriminate 2 sharp points set apart from different distances
  • if subject feels 2 pin pricks, then distance between them is greater than receptive field
  • size of receptive field for any neuron will vary depending on where it is in body
92
Q

What is proprioception?

A
  • imperceptible sixth sense
  • body’s ability to sense movement, action, and location
  • without it you wouldn’t be able to move without thinking about your next step
93
Q

Receptors for proprioception

A
  • golgi tendon organs
  • joint receptors
  • muscle spindles

Proprioceptors are low threshold mechanoreceptors. Piezo2 channels can open when mechanical force is applied

94
Q

Muscle Spindles

A
  • found almost all skeletal muscles
  • 4-8 specialized intrafusal muscle fibers surrounded by capsule of connective tissue
  • positioned parallel and amongst the force-producing fibers of skeletal muscle
  • sensory afferents are coiled around the central part of the intrafusal spindle
95
Q

Muscle Spindle Transduction

A
  1. muscle stretched
  2. tension on intrafusal fiber
  3. activates mechanically gated ion channels in nerve endings
  4. triggers action potential
96
Q

afferent innervation of muscle spindle: two classes of innervation

A
  • primary
  • secondary
97
Q

Primary afferent endings muscle spindle

A
  • largest size axons (Ia)
  • temporal dynamics: rapidly adapting
  • Function: limb dynamics (velocity and direction)

rapidly adapting = can adapt to change in muscle length and speed

98
Q

Secondary afferent endings muscle spindles

A
  • Group II size axons
  • temporal dynamics: slowly adapting
  • function: position sense, postural control, static limb positioning
99
Q

Efferent innervation of muscle spindle

A
  • gamma motor neurons
  • changes in tension impact on sensitivity of the spindle
  • gamma motor neurons ensure muscle spindle contraction occurs if muscle contracts
  • maintains sensitivity of the spindle
100
Q

anatomical distribution of muscle spindles

A
  • large muscles or coarse movement= few spindles
  • fine movement or increased dexterity and/or importance = many spindles
  • no proprioceptive feedback required= no spindles
101
Q

Golgi tendon organs

A
  • branches of Ibeta afferents
  • distributed amongst collagen fibers that form tendons
  • arranged in series with 10-20 extrafusal muscle fibers
  • provides accurate sample of the tension in that particular muscle
102
Q

Joint receptors

A
  • similar to Pacinian corpuscle and ruffini endings
  • originally thought to be main source of proprioceptive info in limbs
  • joint replacements- minor deficits in judging limb position and motion
  • important for finger proprioception; protective role in signaling positions near limits of normal finger joint range of motion
103
Q

Pathways for proprioception

A
  • similarities to tactile: enter through dorsal roots, many fibers also bifurcate into ascending and descending, contain axon collaterals
  • ascending branches travel along the dorsal column
  • some collaterals penetrte dorsal horn of spinal cord and synapse there
104
Q

Pathways for proprioception: cerebellum

A
  • regulates timing of muscle contractions for voluntary movement
  • proprioceptive info required for this function
  • some proprioceptive info reaches higher cortical circuits: some of these axons run through spinal cord tracts whose name reflects their association with this structure
105
Q

Lower body proprioception to cerebellum

A
  • first order proprioceptive afferents - Clarke’s neuron in thoracic spinal cord
  • second order neurons in Clarke’s nucleus - dorsal spinocerebellar tract
  • axon collaterals - third order proprioceptive neurons
  • third order neurons decussate - medial lemniscus
  • medial lemnisucs - VPL
106
Q

Upper body proprioception to brain

A
  • first order neurons travel up dorsal column to medulla
  • synapse in dorsal column nuclei (external cuneate nucleus)
  • second order neurons- ipsilateral cerebellum
  • some branches cross the midline- medial lemniscus- VPL of thalamus
107
Q

Associated somatosensory cortex (SII)

A
  • SII = upper bank of the lateral sulcus
  • convergent info from all subdivisions of SI
  • projects to limbic structures such as the amygdala and hippocampus
  • tactile learning and memory
108
Q

plasticity in adult brain

A
  • peripheral lesion
  • immediately after: corresponding region of cortex is unresponsive
  • after few weeks: area now responsive to stimulation of neighboring regions of skin
  • functional remapping also occurs in thalamus, brainstem, and other cortices
  • cortical representation also changes with experience
  • reversible reorganization of recetpic fields with local anesthetic: area feeling disproportionately large as effects wear off may be a consequence of this change
109
Q

Functional remapping mechanisms

A
  • not known
  • limited value for recovery in some cases: may lead to symptoms that detract, rather than enhance, the quality of life
  • rapid and reversible nature suggests synaptic strength changes of already established synapses are involved: if we could rewire the brain we may be able to reduce the long term impact of acute brain damage
110
Q

Nociception

A
  • pereception of injurious stimuli= nociception
  • it’s leading clinical complaint that can present mystifying symptoms
  • wide range of feeling: can reach intolerable intensity but also disappear quickly
  • universal human experience
111
Q

Specificity vs. convergence

A
  • Specificity: pain is a distinct sensation detected and transmitted by specific receptors and pathways to distinct pain areas of brain
  • Convergence: pain is an integrated, plastic state represented by a pattern of convergent somatosensory activity within a distributed network
112
Q

Specificity aspects

A
  • specifically dedicated receptors and pathways
  • multidimensional response: discriminative, affective, motivational components
113
Q

Convergence aspects

A
  • complex processing- multiple brain areas: brainstem, thalamus, forebrain
114
Q

Nociceptors

A
  • nerve cell endings
  • unspecialized
  • initate the sensation of pain
  • similar to other receptors: stimulus- receptor potential- action potential, cell bodies in dorsal root ganglia, continuous peripheral and central process
115
Q

Nociceptor Categorisation

A
  • lightly myelinated A-alpha fibers: faster (20m/s), mechanosensitive, mechanothermal
  • unmyelinated C fibers: slow (2m/s), polymodal- mechanical, thermal, and chemical

Nociceptors are specific: respond specifically to pain and are a subset of afferents with free nerve endings

116
Q

Fast and Slow Pain

A
  • Fast: first pain, sharp and immediate, A-delta fibers
  • Slow: second pain, more delayed, diffuse and longer lasting pain, C fibers
  • so we can see there are disting set of A-delta and C fiber nociceptors that are specifically associated with pain detection
117
Q

Molecular pain receptors

A
  • activated by heat (and hot chilis)
  • capsaicin receptor: TRPV1, activated at 45C (113F) and by caspacin
  • molecular receptors respond directly to heat so they themselves are the heat detection machines
  • how does capsaicin work: though to mimic endogenous vanilloids released by stressed tissues
  • nociceptors may also work by detecting release of chemicals from stressed cells
118
Q

Central Pain Pathways

A
  • Pathways carrying nociceptive info to the brain are complex
  • 2 components: **sensory discriminative: ** location, intensity, and type of stimulus, involves spinothalamic tract; affective motivational: signals unpleasantness and initiates fight or flight response
119
Q

sensory discriminative pain pathway

A
  • involves spinothalamic tract
  • spinothalamic projections also reserve topography: measure activity in somatosensory cortex indicates: 1. respond to painful stimuli 2. response correlates to intensity 3. spatially mapped info
  • painful stimuli cativate the same region of the somatosensory cortex as non-painful stimuli: also activates a distinct response that includes other regions: insula, cingulate cortex, and connected to the limbic system involved in activation of emotional responses
120
Q

Affective motivational pain pathway

A
  • shares some pathways with anterolateral system
  • little or no topographic mapping
  • number of points of input to limbic and hypothalamic systems
  • strong correlation of painful experience with activity in cingulate cortex
121
Q

Info that supports specified theory:

A
  • there are receptors, both molecular and cellular that respond specifically to pain through subset of fibers
  • there are specific pathways that carry pain messages
  • regions of CNS that are specifically and distinctly activated in response to pain
122
Q

Specified theory misses:

A
  • pain perceived is not always proportional ot intensity of stimulus
  • pain is multi-dimensional
  • modulation can occur by other stimulation (such as acupuncture)
  • perception of pain can occur in severed limbs (phantom limb syndrome)
  • referral of pain from viscera to skin
  • placebo effect
123
Q

sensitization: hyperalgesia

A
  • tissue damage- further stimulus- even more painful
  • this is called hyperalgesia
  • due to changes in neuronal sensitivity in both periphery and centrally
124
Q

inflammatory response- peripheral effects

A
  • tissue damage releases a soup of inflammatory substance
  • affect nerve function, recruit inflammatory cells and molecules, increase local blood flow
  • prostaglandins lower threshold for AP generation
  • some painkillers (analgesics) act on an enzyme important in prostaglandin synthesis
  • afferent neurons activity is being altered bc of tissue damage which gives us our idea of pain
125
Q

Central sensitization

A
  • neurons normally sensitive to non-nociceptive inputs may also become sensitized- normally innocuous stimuli can be perceived as painful
  • Allodynia: outlast the primary painful event by several hours
  • central sensitization can also occur when the central pathways themselves are damaged
  • such neuropathic pain is also sometimes experienced after limb amputation
126
Q
A
127
Q

Phantom Limb Pain

A
  • patients have illusion that limb is still present
  • indicates that central representation of the body persists in absence of peripheral input
  • children can also experience this so this suggests that central maps may be pre-formed
  • pain can also experience through phantom limbs
  • attempts ot block known pain pathways usually fail, suggesting this pain may also be centrally represented
  • suggests the pain we experience may in part be what we expect it to be
128
Q

Referred Pain

A
  • pain in viscera felt as coming from specific region of skin
  • Thought to reflect convergence of visceral afferents onto similar pathways as cutaneous afferents in CNS
  • extremely useful however in aiding clinical diagnosis of organ dysfunction
129
Q

Central modulation of pain

A
  • perception of pain varies according to context
  • WWII soldiers- involuntary
  • walking on hot coals- voluntary
  • placebo effect
  • indicates that mechanism exists, voluntary or involuntary, to overcome severe pain
130
Q

local modulation of pain

A
  • rubbing on an injury often relieves pain
  • thought to be due to local inhibition by mechanoreceptors of nociceptive inputs in spinal cord
131
Q

Pain pathways

A
  • branch into ascending and descending collaterals
  • enter spinal cord via dorsal roots
  • cell body in dorsal root ganglia
  • forms the dorsolateral tract of lissauer
132
Q

Lissauer’s Tract

A
  • branches contact second order neurons located in Rexed’s laminae I, II, and V
  • Laminae I and V = contain projection neurons whose axons travel to the brainstem and thalamic targets
  • abundant interneurons in laminae II which are afferent terminations
133
Q

Laminae of spinal cord

A
  • C fibers: terminate in laminae I and II
  • A-delta fibers: I and V
  • A-beta fibers: III, IV, and V
  • some neurons in laminae V receive both nociceptive and non-nociceptive inputs: callled wide-dynamic range neurons, receive visceral sensory input so these are the likely cause of referred pain

Systems of Neuroscience (2 decks)

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